I have been fascinated by atrial fibrillation since I was a
third-year medical student. I was doing a Medicine rotation and examining a
middle-aged man. Listening to his heart
sounds was the first time I heard the irregularly irregular heart rhythm characteristic
of atrial fibrillation. It was such an outrageous and unexpected sound compared
to what I was used to that I felt a little panicky. Why wasn’t this patient
experiencing more symptoms and even more unexplainably – why doesn’t he sense
that there is something wrong with his heart beat? Since then, I have treated hundreds of
patients with atrial fibrillation. I ask
them all if they can sense the irregular heart beat and in the people I see
about half of them can. Being a
psychiatrist, diagnosing and treating atrial fibrillation is technically not my
“job”. But it is currently such a
prevalent condition that a brief examination typically triggered by vital signs
and noting a pulse irregularity followed by an electrocardiogram is all that is
needed. Atrial fibrillation has considerable mortality and morbidity associated
with the most feared complication of stroke. A good friend of mine developed renal
failure from a combination of atrial fibrillation and atrial flutter and
required ablation procedures to restore normal sinus rhythm. Two relatives had strokes associated with
atrial fibrillation resulting in disability and ultimately death. Both had atrial fibrillation for about 30 years. One of them was 92 years old, using digoxin for rate control, and not on anticoagulants. The other was 92 years old, using diltiazem for rate control, and on warfarin at therapeutic doses. He had two strokes about 10 years apart on the warfarin and multiple episodes of nuisance bleeding or excessive bleeding from minor injuries due to anticoagulation that did not require medical attention. Another
friend had pulmonary complications from an antiarrhythmic drug that he was
taking for a new onset of atrial fibrillation and died as a result of those complications. Sixteen years ago – I developed
lone atrial fibrillation while speedskating and have been on antiarrhythmics
since that time.
When you see all of those problems associated with a
condition and have had it yourself, you tend to read more about it than the
average person. Reading about atrial
fibrillation is generally a frustrating task. The evidence base for treating
the condition seems to be in a state of flux. For years the research seemed to
say that rate control and rhythm control led to equivalent outcomes. When life
style measures were included, the rhythm control strategies seemed superior.
Even the question of anticoagulation with novel oral anticoagulants of NOACs
for stroke prevention based on a scoring system has been called into question recently.
That brings me to the topic of this blog post and that is
the single best summary of information about atrial fibrillation that I have
seen anywhere - at least for nonspecialists in that area.
The paper was written this year in the New England Journal
of Medicine (1). It starts out with a case description of a 63-year-old man with a
new onset of atrial fibrillation. The authors discuss the disease in detail and
treatment recommendations consistent with their discussion. What I really like
about this paper is that they are discussing phenotypes of atrial fibrillation
and I do not see that happening very often in real clinical situations. The
phenotypes they discuss are paroxysmal atrial fibrillation, persistent
atrial fibrillation, and long-standing persistent atrial
fibrillation. They have an excellent
figure in their paper that was unfortunately prohibitively expensive for me to
try to post here, but the basic idea is that there are distinct anatomical and
electrophysiological substrates for each of those phenotypes. In the paper the
phenotypes are labeled as “clinical profiles”. His phenotypes have prognostic
considerations since the authors make the point that there is a gradation in
the likelihood of conversion to normal sinus rhythm and maintaining that
rhythm with paroxysmal atrial fibrillation being the most likely to convert and
maintain a normal sinus rhythm and long-standing persistent atrial fibrillation
being the least likely to convert. Just knowing that much about atrial
fibrillation is a significant advance compared with most of the clinical discussions
that I hear.
The second feature in this paper that I really like is that
atrial fibrillation is not necessarily a benign condition. For years the
discussion has been controlling the rate or rhythm and in most cases they have
been considered to be equivalent. Many clinicians have their first experience
with atrial fibrillation like I had. They are doing a physical examination
outpatient for another reason and they notice they are in atrial fibrillation.
Depending on physiological factors that patients irregularly irregular heart
rate may already be rate controlled. I have talked with many people over the
years who knew that their heart rate was irregular because their spouse noticed
it and they did not do anything about it for years. Atrial fibrillation is a risk factor
for embolic strokes as well as dementia, death, and heart failure. Persistent
tachycardia can cause cardiomyopathy and reduced cardiac output can lead to
renal failure. The authors suggest that
a heart rate of 110 bpm or greater might lead to cardiomyopathy but they also
suggest it can occur at a lower rate. This is an interesting observation
because the most recent review in UpToDate on sinus tachycardia suggests it is
generally a benign condition, however an irregular tachycardia because of
reduced cardiac output is likely a different matter.
In addition, the patient can be symptomatic from reduce
cardiac output with lightheadedness, dizziness, fatigue, decreased exercise
tolerance, palpitations, hypertension, and an exacerbation of symptoms of underlying coronary
artery disease. The lesson for psychiatrists is if you notice that a patient
has atrial fibrillation it cannot be approached casually. Atrial fibrillation
is associated with significant medical comorbidities such as underlying
structural coronary disease, obesity, sleep apnea, hypertension,
hyperlipidemia, and diabetes mellitus. If the patient has had limited contact
with primary care physicians the comorbid conditions may have gone unnoticed.
It makes sense to ask about additional symptoms in the review of systems as
well as family history and whether that patient is seen primary care physician
or cardiologist recently. I would have
no problem referring a patient with tachycardia, expected symptoms, or risk factors to
an emergency department for acute stabilization if I could not get them seen in
a primary care clinic.
The authors go into treatment of atrial fibrillation as
basically a rate control strategy, a rhythm control strategy, and a strategy to
address comorbid medical conditions. They
review rate control with beta-blockers and calcium channel blockers and prefer
beta-blockers. They consider a number of antiarrhythmics and the risks and
benefits of those medications. They
consider catheter ablation - either radiofrequency pulmonary vein isolation or
cryoablation as being more effective for treating and preventing recurrent
atrial fibrillation. The recurrence rates are relatively high even after the
ablation procedures, so continued antiarrhythmic medications may be necessary.
Once a patient has stable treated atrial fibrillation, the
main task for the psychiatrist is to make sure that any prescribed medications
do not interfere with the cardiac medications at either the pharmacokinetic or
pharmacodynamic level. QTc prolongation is a primary consideration since
several of the agents used prolong the QTc interval or affect other cardiac conduction. At the pharmacokinetic level there is the
possible risk of decreased metabolism of beta-blockers and increasing
bradycardia and hypotension. If I have any doubts all about medication
combinations I am usually in touch with the patient’s cardiologist or primary
care physician before making those changes. All of the patients I see with
atrial fibrillation also have their blood pressure and pulse taken at every visit
along with the description of symptoms and potential medication side effects. That means I never practice in an environment where I can't do that. I
will also review how well their comorbid conditions are being treated
particularly hypertension, sleep apnea, and diabetes mellitus. I will provide
them with concrete advice on how to approach those problems and whether or not
they need to be seeing their primary care physician sooner than scheduled.
This is also an opportunity to discuss any comorbid
substance use problems. Alcohol is a definite precipitant of atrial
fibrillation. I have had patients never experience another episode by stopping
alcohol. I have also had patients report that they can tell when their alcohol level reaches a certain point because they will go into atrial
fibrillation for several hours until that alcohol is metabolized. Stimulant
medications are also a risk because they increase sympathetic tone, increase
heart rate, increase blood pressure. All three of those changes can trigger an
episode of atrial fibrillation. Cannabis
can have a fairly potent sympathomimetic effect by acutely lowering blood
pressure leading to a reflex tachycardia. Atrial fibrillation has been reported as one of several cardiac
arrhythmias associated with cannabis use (2). Interestingly, the authors of the
NEJM article state that caffeine is not a precipitant. There are no qualifiers
on that statement and I think it is based primarily on epidemiological
evidence. Caffeine intake is always important to quantify because of its wide
variability across the population and general reputation of being a benign compound. There are
segments of the population that consume large quantities of caffeinated
beverages every day and experience the expected side effects of anxiety (in
some cases panic attacks), agitation, insomnia, and hyperadrenergic effects but they seem
unaware that these symptoms are related to their caffeine consumption.
Certainly consumption at that level can directly or indirectly precipitate an episode of atrial fibrillation.
That is my brief review of the NEJM article in atrial
fibrillation. I encourage all psychiatrists to get a copy of this paper, read
it, and keep it for reference. I am not suggesting that psychiatrists treat this condition. I am suggesting that they recognize it - even if it has not been diagnosed and know what to do when that occurs. The reality is that in adult psychiatry no matter
what your practice setting there will be a significant number of people with
atrial fibrillation and other arrhythmias as well as all of the known comorbidities.
You cannot treat those people unless you know about these conditions, the
comorbidities, and how to avoid complications.
George Dawson, MD, DFAPA
References:
1: Michaud GF,
Stevenson WG. Atrial Fibrillation. N Engl J Med. 2021 Jan 28;384(4):353-361.
doi: 10.1056/NEJMcp2023658. PMID: 33503344.
2: Richards JR,
Blohm E, Toles KA, Jarman AF, Ely DF, Elder JW. The association of cannabis use
and cardiac dysrhythmias: a systematic review. Clin Toxicol (Phila). 2020
Sep;58(9):861-869. doi: 10.1080/15563650.2020.1743847. Epub 2020 Apr 8. PMID:
32267189.
Supplementary:
Common and uncommon medications listed in this article used in atrial fibrillation for rate control, antiarrhythmic properties, and anticoagulation. I added additional warnings and general type of medications that might require avoiding based on pharmacokinetic or pharmacodynamic considerations. Important to keep in mind that all medications vary in their ability to affect these mechanisms as well as therapeutic mechanisms. That includes significant differences between medications in the same class. That leads to qualifiers like "all possible mechanisms leading to complications or serious adverse effects may not be listed" (in this package insert or computerized drug interaction program). Almost every time I am seeing a patient on these medications - it requires a study of the medication combination, even if they are taking a psychiatric medication that appears to be working. Baseline cardiac symptoms related to the arrhythmia also need to be established as well as the patient's plan to obtain assistance if they worsen.
Additional qualifier (if it is not obvious). Psychiatrists prescribe beta blockers (metoprolol, propranolol, pindolol, etc). Psychiatrists can diagnose atrial fibrillation. Psychiatrists do not manage atrial fibrillation but need to know what to do acutely and how to avoid complications of the following medical therapies from drug interactions with psychiatric medications. Practically all of the antiarrhythmics in the following table are prescribed by Cardiologists and subsequently managed by primary care physicians although many patients continue to see Cardiologists in follow up. Like all areas of medicine the limits of technical expertise need to be recognized. I worked with Cardiologists who became psychiatrists and they restricted their practice to medications prescribed by psychiatrists.
Graphics Credit:
Bunch TJ, Cutler MJ. Is pulmonary vein isolation still the cornerstone in atrial fibrillation ablation? J Thorac Dis 2015;7(2):132-141. doi: 10.3978/j.issn.2072-1439.2014.12.46
Open Access per this Creative Commons License: https://creativecommons.org/licenses/by-nc-nd/4.0/
